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Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [scRNA-seq]

ABSTRACT: Sepsis, a worldwide health crisis, is notorious for its high mortality rate, often attributed to the development of acute lung injury. The direct migration of intestinal immune cells to the lung as a mediator of acute lung injury remains unclear. Our study unveiled a process where cecal ligation and puncture-induced sepsis prompted a migration of γδT cells from the small intestine to the lung, subsequently triggering an overwhelming inflammatory response dominated by IL-17A.

ORGANISM(S): Mus musculus

PROVIDER: GSE266493 | GEO | 2024/06/14

REPOSITORIES: GEO

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Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [ChIP-seq]

Project description:Sepsis, a worldwide health crisis, is notorious for its high mortality rate, often attributed to the development of acute lung injury. The direct migration of intestinal immune cells to the lung as a mediator of acute lung injury remains unclear. Our study unveiled a process where cecal ligation and puncture-induced sepsis prompted a migration of γδT cells from the small intestine to the lung, subsequently triggering an overwhelming inflammatory response dominated by IL-17A.

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Sepsis-induced acute lung injury is exacerbated by pulmonary Wnt signaling-dependent migration of small intestinal memory γδT17 cells to the lung

Project description:Sepsis, a worldwide health crisis, is notorious for its high mortality rate, often attributed to the development of acute lung injury. In this context, the lung, being particularly vulnerable to septic damage, emerge as a primary battleground. The possible roles of the gut-lung axis mediated by the gut microbiota and its metabolic products in the context of acute lung injury have been documented. However, the direct migration of intestinal immune cells to the lung as a mediator of acute lung injury remains unclear. Our study unveiled a process where cecal ligation and puncture-induced sepsis prompted a migration of γδ T cells from the small intestine to the lung, subsequently triggering an overwhelming inflammatory response dominated by IL-17A. Small intestinal memory γδT17 cells (CD44+ IL-7Rhigh CD8low Ly6C–) were the major subtype of γδ T cells that migrated from the small intestine to the lung and aggravated acute lung injury. Moreover, the activation of the Wnt signaling in the alveolar macrophages during sepsis was identified as a driving factor for the subsequent CCL1 upregulation, which prompted the migration of small intestinal memory γδT17 cells to the lung. S-Ketamine (S-KT) treatment demonstrated a notable capacity to alleviate acute lung injury through dampening pulmonary Wnt/β-catenin signaling-mediated migration of small intestinal γδT17 cells to the lung. Our findings highlight the significant contribution of the direct migration of immune cells from the small intestine to the lung in sepsis-induced acute lung injury, and clrify the pathological significance of the localized elevation of IL-17A in the lung.

2024-04-24 | PXD051763 |

Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [ChIP-seq]

Project description:Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [ChIP-seq]

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Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [scRNA-seq]

Project description:Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury [scRNA-seq]

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Project description:sepsis-induced acute lung injury

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Antigen-presenting aged neutrophils induce CD4+ T cells to exacerbate inflammation in sepsis

Project description:Extracellular cold-inducible RNA-binding protein (eCIRP) is a key mediator of severity and mortality in sepsis. We found that stimulation of mouse bone marrow–derived neutrophils (BMDNs) with eCIRP generated a distinct neutrophil subpopulation, characterized by cell surface markers of both antigen-presenting cells and aged neutrophils as well as expression of IL-12, which we named antigen-presenting aged neutrophils (APANs). The frequency of APANs was significantly increased in the blood, spleen, and lungs of WT mice subjected to cecal ligation and puncture–induced sepsis but not in CIRP–/– mice. Patients with sepsis had a significant increase in circulating APAN counts compared with healthy individuals. Compared with non–APAN-transferred mice, APAN-transferred septic mice had increased serum levels of injury and inflammatory markers, exacerbated acute lung injury (ALI), and worsened survival. APANs and CD4+ T cells colocalized in the spleen, suggesting an immune interaction between these cells. APANs cocultured with CD4+ T cells significantly induced the release of IFN-γ via IL-12. BMDNs stimulated with eCIRP and IFN-γ underwent hyper-NETosis. Stimulating human peripheral blood neutrophils with eCIRP also induced APANs, and stimulating human neutrophils with eCIRP and IFN-γ caused hyper-NETosis. Thus, eCIRP released during sepsis induced APANs to aggravate ALI and worsen the survival of septic animals via CD4+ T cell activation, Th1 polarization, and IFN-γ–mediated hyper-NETosis.

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Single-cell RNA-seq of Bronchoalveolar Lavage Fluid Immune Cells from Padi2/Padi4 Double Knock-out Mice in Pseudomonas aeruginosa Pneumonia-induced Sepsis

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